Multiple sclerosis (MS) as a chronic inflammatory disorder of the central nervous system (CNS) is thought to be caused by the abnormal induction of immune responses. Chemokines as molecules that can engage leukocytes into the location of inflammation, actively participate in the pathogenesis of MS. Several members of this family of chemo attractants have been shown to be dysregulated in the peripheral blood, cerebrospinal fluid or CNS lesions of MS patients. Studies in animal models of MS particularly experimental autoimmune encephalomyelitis have indicated the critical roles of chemokines in the pathophysiology of MS. In the current review, we summarize the data regarding the role of CCL2, CCL3, CCL4, CCL11, CCL20, CXCL1, CXCL2, CXCL8, CXCL10, CXCL12 and CXCL13 in the pathogenesis of MS.

多发性硬化症 (MS) 作为中枢神经系统 (CNS) 的一种慢性炎症性疾病，被认为是由免疫反应的异常诱导引起的。趋化因子作为可以使白细胞进入炎症位置的分子，积极参与 MS 的发病机制。该化学引诱剂家族的几个成员已被证明在 MS 患者的外周血、脑脊液或 CNS 病变中失调。MS 动物模型，特别是实验性自身免疫性脑脊髓炎的研究表明，趋化因子在 MS 的病理生理学中起着关键作用。在本综述中，我们总结了有关 CCL2、CCL3、CCL4、CCL11、CCL20、CXCL1、CXCL2、CXCL8、CXCL10、CXCL12 和 CXCL13 在 MS 发病机制中的作用的数据。